Cardio: First Aid Step 1 2010

Front 1

most posterior part of heart?
clinical impact?

Back 1

Left Atrium.
LA enlargement -> dysphagia (compressing esohpagus) or hoarseness (compression of recurrent laryngeal n)

Front 2

CO measurement? (Fick Principle)

Back 2

rate of O2 consumption / (arterial O2 content - venous O2 content)

Front 3

myocardial O2 demand increases by what 4 factors?

Back 3

increased afterload (aortic pressure)
increased contractility
increased HR
increased heart size (increase wall tension)

Front 4

what 3 factors affect SV and how

Back 4

SV CAP (contractility, afterload, preload)

increased SV when:
increase contractility and preload
decrease afterload

Front 5

Hydralazine

Back 5

vasodilator, decreases afterload (hydrAlAzine: afterload, arterial)

Front 6

Nitroglycerin

Back 6

VENOdilator (decreases preload)

Front 7

What states increase viscosity

Back 7

polycythemia, hyperproteinemic states (e.g., MM), hereditary spherocytosis

Front 8

what phase of cardiac cycle has highest O2 consumption

Back 8

isovolumetric contraction

Front 9

S3

Back 9

EARLY diastole, common in dilated ventricle (NL in children and pregnant women)

Front 10

S4

Back 10

("atrial kick"), LATE diastole
assoc w/ventricular hypertrophy (LA must push against stiff LV wall) restricted and hypertrophic cardiomyopathy

Front 11

paradoxical splitting

and what causes it?

Back 11

aortic stenosis or LBBB (states that delay LV empyting)
P2 before A2
on inspiration, NO split as P2 moves towards A2

Front 12

Fixed splitting

Back 12

ASD (L to R shunt increased flow thru pulmonic valve; P2 delayed regardless of inspiration)

Front 13

Wide splitting

Back 13

pulmonic stenosis or RBBB (states that delay RV empyting)
exaggeration of NL splitting
delayed P2 regardless of breathing

Front 14

Phase 0 upstroke in ventricular AP?

Phase 0 upstroke in SA/AV node?

Back 14

voltage-gated Na channels

voltage-gated Ca channels

Front 15

Phase 4 in SA node

Back 15

determines HR, accounts for automaticity of SA/AV nodes
If channels

Front 16

U wave on ECG

Back 16

caused by hypokalemia and bradycardia

Front 17

ST segment

Back 17

ventricle completely depolarized (isoelectric)

Front 18

Order of speed of conduction through cardiac circuit (fastest to slowest)

Back 18

Purkinge > atria > ventricles > AV node

Front 19

Jervell and Lange-Neilsen syndrome

Back 19

congenital long QT syndromes,
most often due to defects in cardiac Na or K channels,
can present w/sensorineural deafness

Front 20

Wolff-Parkinson-White syndrome

Back 20

ventricular pre-excitation syndrome, an accessory conduction pathway from atria to ventricles (bundle of Kent) that bypasses AV node,
ventricles partiallly depolarize earlier -> characteristic delta wave,
can lead to reentry current -> SVT

Front 21

A Fib?
Clinical consequence?
Trx?

Back 21

irregularly irregular, no discrete P waves inb/w irregularly spaced QRS complexes

atrial stasis, leading to stroke

B-blockers or Ca-channel blockers; prophylaxis against TE (thromboembolism) w/warfarin (Coumadin)

Front 22

How do you treat Atrial Flutter?

Back 22

Class IA, IC, or III antiarrhythmics

Front 23

1st degree AV block

Back 23

Asymptomatic

PR interval prolonged (> 200 msec)

Front 24

2nd degree AV block Type 2 (Mobitz)

Back 24

pathologic condition (unlike Type 1: Wenckebach)

can progress to 3rd degree block

Front 25

3rd degree AV block

What do you treat it with?

Back 25

atria and ventricles beat independently of each other

atrial rate faster than ventricular rate

Trx w/pacemaker

Front 26

What dz can cause 3rd degree heart block

Back 26

Lyme disease

Front 27

ANP

Back 27

involved in "escape from aldosterone" mechanism

diuretic, causing generalized vascular relaxation

released in response to increased blood volume and atrial pressure

Front 28

aortic arch receptors

carotid sinus receptors

Back 28

aortic arch: responds ONLY to increase in BP (via CN X to medulla)

carotid sinus: responds both to increase and decrease in BP (via CN IX to solitary nucleus in medulla)

Front 29

Cushing triad

Back 29

HTN, bradycardia, respiratory depression

Front 30

Cushing reaction

Back 30

due to central chemoreceptors in brain

increased ICP constricts arterioles -> cerebral ischemia -> HTN (sympathetic response) -> reflex bradycardia

Front 31

PCWP (pulmonary capillary wedge pressure)

what happens in mitral stenosis?

Back 31

good approx of L atrial pressure

PCWP > LV diastolic pressure

Front 32

What are the R to L shunts?

What do R to L shunts cause?

Back 32

The 5 T's (Tetralogy, Transposition, Truncus arteriosus, Tricuspid atresia, TAPVR)

early cyanosis ("blue babies")

Front 33

What is TAPVR (total anomalous pulmonary venous return)

Back 33

pulmonary veins drain into R heart circulation

Front 34

What are the L to R shunts?

What do they cause?

What can they progress to?

Back 34

VSD > ASD > PDA

late cyanosis ("blue kids")

Eisenmenger's syndrome (arteriolar thickening/vascular hypertrophy from increased pulm resistancce -> progressive pulm HTN -> shunt reverses to R to L -> late cyanosis--clubbing and polycythemia)

Front 35

What causes Tetralogy of Fallot

Back 35

anterosuperior displacement of the infundibular septum

Front 36

How do pts w/Tetralogy of Fallot present (grossly, not characteristics of tetralogy)

Back 36

patients squat to improve Sx

compression of femoral arteries increase Pressure -> decreasing R to L shunt -> directing more flow from RV to lungs

Front 37

What causes Transposition of the great vessels

Back 37

failure of aorticopulmonary septum to spiral

need a shunt in order to survive

Front 38

infantile type vs adult type (coarctation of aorta)

clinical manifestations?

Back 38

infantile is proximal to insertion of ductus arteriosus (preductal); adult is distal to it (postductal)

HTN in upper extremities, weak pulses in LE; assoc w/ Turner's syndrome; can result in aortic regurgitation, most commonly assoc w/bicuspid aortic valve

Front 39

PDA

Back 39

in fetal period, R to L shunt was NL

in neonatal period, lung resistance decreases and shunt becomes L to R w/RVH and failure

Indomethacin closes it; PGE keeps it open

Front 40

Congenital Cardiac Defects

22q11 syndromes
Down syndrome
Congenital Rubella
Turner's
Marfan's
Infant of diabetic mother

Back 40

22q11: Truncus arteriosus, Tetralogy
Down: endocardial cushion defects (ASD, VSD, AV septal defect)
Rubella: septal defects, PDA, pulm artery stenosis
Turner's: coarctation
Marfan's: aortic insufficiency (late)
Diabetic: Transposition of great vessels

Front 41

Monckeberg atherosclerosis

Back 41

calcification in media of radial and ulnar arteries, especially
does NOT obstruct blood flow and intima is NOT involved

Front 42

arteriolosclerosis

Back 42

hyaline thickening or proliferative changes in small arteries in essential HTN or DM

hyperplastic: "onion-skinning" in malignant HTN (in kidneys, called malignant nephrosclerosis)
hyaline: hyaline thickening of walls (in kidneys, benign nephrosclerosis)

Front 43

pathogenesis of atherosclerosis

Back 43

endothelial cell dysfxn -> macrophage and LDL accumulation -> foam cell formatiion -> fatty streaks -> smooth m cell migration (involves PDGF and FGF-beta) -> fibrous plaque -> complex atheroma

Front 44

Dressler's syndrome

Back 44

autoimmune phenomenon resulting in fibrinous pericarditis (several weeks post MI)

Front 45

etiologies of DCM

Back 45

ABCCCD
Alcohol Abuse, wet Beriberi, Coxsackie B virus myocarditis, chronic Cocaine use, Chagas' dz, Doxorubicin toxicity

hemochromatosis and peripartum cardiomyopathy

Front 46

DCM vs Hypertrophic cardiomyopathy

What is clinical risk assoc w/hypertrophic cardiomyopathy?

Back 46

DCM: systolic dysfxn, eccentric hypertrophy (sarcomeres in series), most common

Hypertrophic: diastolic dysfxn, concentric hypertrophy (sarcomeres in parallel)

Risk w/hypertrophic: proximity of hypertrophied IV septum to mitral leaflet obstructs outflow tract -> systolic murmur and syncopal episodes

Front 47

How do you trx Hypertrophic cardiomyopathy?

Back 47

B-blockers or non-DHP Ca-channel blockers (like verapamil)

Front 48

Causes of restrictive cardiomyopathy

Back 48

Sarcoidosis, amlyoidosis, postradiation fibrosis, Loffler's syndrome, hemochromatosis (hemochromatosis also in DCM)

-restrictive has diastolic dysfxn, like hypertrophic

Front 49

What is Loffler's syndrome?

Back 49

endomyocardial fibrosis w/ a prominent eosinophilic infiltrate)

Front 50

Tricuspid valve endocarditis

What organisms are assoc?

Back 50

assoc w/ IV drug abuse

assoc w/S. aureus, Pseudomonas, Candida

Front 51

acute bacterial endocarditis

subacute endocarditis

Back 51

acute: S. aureus (high virulence), large vegetations on previously NL valves

subacute: viridans streptococci (low virulence), smaller vegetations on congenitally abNL or diseased valves, sequela of dental procedures

Front 52

Features of bacterial endocarditis?

Complications of it?

Back 52

Features: Bacteria FROM JANE
(fever, Roth spots, Osler's nodes, new Murmur, Janeway lesion's, Anemia, Nail-bed/splinter hemorrhages, Emboli)

Comps: chordae rupture, glomerulonephritis, suppurative pericarditis, emboli

Front 53

Libman-Sacks endocarditis

Back 53

verrucous (wart-like), sterile vegetations on BOTH sides of valve, assoc w/mitral stenosis

most common heart manifestation of SLE

Front 54

Features of Rheumatic heart disease

Back 54

FEVERSS
Fever, Erythema marginatum, Valvular damage (vegetation and fibrosis), increased ESR, Red-hot joints (migratory polyarthritis), Subcutaneous nodules (Aschoff bodies), St. Vitus' dance (chorea)

Front 55

Janeway lesions

Osler's nodes

Back 55

Janeway: small erythematous lesions on palm or sole)

Osler's: tender raised lesions on finger or toe pads

Front 56

States where you see pulsus paradoxus

Back 56

severe cardiac tamponade, asthma, OSA, pericarditis, croup

Front 57

Kussmaul's sign (and what are they associated with)

Kussmaul's pulse

Back 57

sign: increase in JVP on inspiration (assoc w/cardiac tumors)

pulse: exaggerated decrease in amplitude of pulse during inspiration

Front 58

Osler-Weber-Rendu syndrome/Hereditary hemorrhagic telangiectasia

Back 58

AD inheritance

recurrent epistaxis, skin discolorations, mucosal telangiectasias, GI bleeds

affects small vessels

Front 59

weak pulses in upper extremities

Back 59

Takayasu's arteritis

Front 60

Henoch-Schonlein purpura

Back 60

most common form of childhood systemic vasculitis,
skin rash on buttocks and legs (palpable purpura), arthralgia, intestinal hemorrhage, ab pain and melena

assoc w/IgA nephropathy

triad: skin, joints, GI

Front 61

Auscultation and location:
Aortic area

Back 61

2nd R intercostal space

Systolic murmur (aortic stenosis, flow murmur, aortic valve sclerosis)

Front 62

Auscultation:
Pulmonic area

Back 62

2nd L intercostal space

Systolic ejection murmur (pulmonic stenosis, flow murmur)

Front 63

Auscultation and location:
Tricuspid area

Back 63

4th intercostal space

Pansystolic murmur (tricuspid regurg, VSD)

Diastolic murmur (tricuspid stenosis, ASD)

Front 64

Auscultation and location:
Mitral area

Back 64

5th intercostal space

Systolic murmur (mitral regurg)

Diastolic murmur (mitral stenosis)

Front 65

Auscultation:
Left sternal border

Back 65

Diastolic murmur (aortic or pulmonic regurg)

Systolic murmur (hypertrophic cardiomyopathy)

Front 66

MR/TR

Back 66

Holosystolic, high-pitched "blowing" murmur

Front 67

MR

and what can cause it

Back 67

loudest as apex radiating to axilla,
enahnced by manuevers that increase TPR (squatting, hand grip) or increase LA return (expiration),

often due to IHD, MVP or LV dilation

Front 68

TR

Back 68

loudest at tricuspid area and radiates to R sternal border, enhanced by manuevers that increase RA return (inspiration)

due to RV dilation or endocarditis (Rheumatic fever can cause both)

Front 69

Aortic stenosis

Back 69

crescendo-decrescendo systolic ejection murmur following an ejection click, radiates to carotids/apex,
LV >> aortic pressure during systole

"pulsus parvus et tardus": pulses weak compared to heart sounds -> syncope

due to age-related calcific aortic stenosis or bicuspid aortic valve

Front 70

VSD

Back 70

holosystolic, harsh-sound murmur

loudest at tricuspid area

Front 71

MVP

Back 71

late systolic crescendo murmur w/midsystolic click (MC),
loudest at S2,
most common valvular lesion,
enhanced my maneuvers that increase TPR (like MR)

Front 72

What are etiologies of MVP

Back 72

myxomatous degeneration, rheumatic fever or chordae rupture

Front 73

Aortic regurg

Back 73

immediate high-pitched "blowing" diastolic murmur, can have wide PP if chronic,
due to aortic root dilation, bicuspid aortic valve or rheumatic fever

can present w/bounding pulses and head bobbing

Front 74

Mitral stenosis

Back 74

follows opening snap (OS), delayed rumbling late diastolic murmur, LA >> LV pressure during diastole

enhanced by maneuvers that increase LA return (expiration)

often 2ndary to rheumatic fever

chronic MS can -> LA dilation

Front 75

PDA

Back 75

continuous machine-like murmur, loudest at S2

Front 76

Triad of Wegener's granulomatosis

Back 76

focal necrotizing vasculitis, necrotizing granulomas in lung and upper airway, necrotizing glomerulonephritis

Front 77

Sturge-Weber dz

Back 77

port-wine stain on face (nevus flammeus), ipsilateral leptomeningeal angiomatosis (intracerebral AVM), early-onset glaucoma

Front 78

Kawasaki dz

Back 78

acute, self-limiting necrotizing vasculitis in infants/children

assoc w/Asian ethnicity

strawberry tongue, desquamative skin rash, fever, conjunctivitis, can develop coronary aneurysms

Front 79

PAN

Back 79

immune complex-mediated transmural vasculitis w/fibrinoid necrosis

Hep B seropositivity in 30%, multiple aneurysms and constrictions on arteriogram

involves renal and visceral vessels, NOT pulmonary aa

Front 80

Takayasu's arteritis

Back 80

"pulseless dz," granulomatous thickening of aortic arch and/or proximal great vessels

increased ESR, mainly affects Asian females

FAN MY SKIN On Wednesday (Fever, Arthritis, Night sweats, MYalgia, SKIN nodules, Ocular disturbances, Weak pulses in UE)

affects medium and large arteries

Front 81

Temporal arteritis

Back 81

(giant cell arteritis)
most common vasculitis affecting medium and large arteries (usually branches of carotid), affects elderly females

focal, granulomatous inflammation

jaw claudication, unilateral headache, impaired vision (occlusion of ophthalmic artery that may lead to irreversible blindness)

increased ESR, and 1/2 of pts have systemic involvement and Polymylagia Rheumatica

Front 82

Strawberry vs Cherry hemangioma

Back 82

Strawberry: in infancy, grows w/child and spontaneously regresses

Cherry: elderly and do NOT regress, frequency increases w/age

Front 83

Bacillary angiomatosis

Back 83

benign skin papules in AIDS pts

caused by Bartonella henselae infections

frequently mistaken for Kaposi's sarcoma

Front 84

angiosarcoma

Back 84

highly lethal malignancy of liver

assoc w/vinyl chloride, Thorotrast (ThO2) exposure, arsenic

Front 85

lymphangiosarcoma

Back 85

lymphatic malignancy assoc w/persistent lymphedema (e.g., postradical mastectomy)

Front 86

Trx: Wegener's granulomatosis

Back 86

Cyclophosphamide and corticosteroids (same as PAN)

Front 87

Trx: Buerger's dz

Back 87

smoking cessation

Front 88

Trx: PAN

Back 88

Corticosteroids, cyclophosphamide (same as Wegener's)

Front 89

Trx: Kawasaki's

Back 89

IVIg, aspirin

Front 90

Trx: temporal arteritis

Back 90

high-dose steroids

Front 91

Small vessel vasculitides

Back 91

Wegener's, other ANCA-positive vasculitides, Sturge-Weber, HSP

medium too: Buerger's, Kawasaki, PAN

Front 92

Medium vessel vasculitides

Back 92

(small too): Buerger's, Kawasaki, PAN

(large too): Takayasu's, Temporal arteritis

Front 93

Large vessel vasculitides

Back 93

Takayasu's, Temporal arteritis (both affect medium vessels too)

Front 94

Other ANCA-positive vasculitides

Back 94

Microscopic polyangitis (p-ANCA), primary pauci-immune crescentic GN, Churg-Strauss dz (p-ANCA)

Front 95

Wegener's vs Churg-Strauss (clinical)

Back 95

Wegener's: hemoptysis, hematuria, perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis, cough, dyspnea (c-ANCA)

Churg-Strauss: (granulomas w/eosinophilia), asthma, sinusitis, skin lesions, peripheral neuropathy (wrist/foot drop), can involve heart, GI, kidney (p-ANCA)

Front 96

Hyperlipidemia and how it influences atherosclerosis

Back 96

may initiate endothelial injury

promote foam cell formation, act as a chemotactic factor for monocytes, inhibit macrophage motility, injure smooth m cells

Front 97

atherosclerotic aneursym

Back 97

most frequently in descending, esp abdominal, aorta

Front 98

berry aneurysms

Back 98

unr/t atherosclerosis

develop at sites of congenital medial weakness (bifurcation of cerebral aa), so not present at birth

most frequent cause of subarachnoid hemorrhage

Front 99

Syphilitic (luetic) aneurysm

Back 99

caused by syphilitic aortitis (obliterative endarteritis of vasa vasorum and media necrosis), grossly looks like a "tree-bark" appearance

more in ascending aorta (vs descending for atherosclerosis) -> dilation -> aortic insufficency

Front 100

Dissecting aneurysm

Back 100

longitudinal intraluminal tear in ascending aorta, forming a 2nd lumen w/in media

-confused w/MI, but ECG and enzymes all NL

-results in aortic rupture, most often into pericardial sac, -> hemopericardium and fatal cardiac tamponade

assoc w/HTN and cystic medial necrosis, not r/t atherosclerosis

Front 101

spider telangiectasia

Back 101

assoc w/hyperestrinsim, like in chronic liver dz or pregnancy

Front 102

cavernous hemangioma

Back 102

can occur in von Hippel-Lindau dz (AD disorder marked by hemangioblastomas of cerebellum, brain stem and retina; adenomas and cysts of liver/kidney/pancreas, etc.; increased incidence of RCC)

Front 103

lymphomatoid granulomatosis

Back 103

rare granulomatous vasculitis

infiltration by atypical lymphocytoid and plasmacytoid cells

-can go from chronic inflammatory condition to lymphoproliferative neoplasm (most often T cell non-Hodgkin lymphoma)

Front 104

causes of renal HTN

Back 104

disorders of renal parenchyma

unilateral renal artery stenosis (can be from atherosclerosis or unilateral fibromuscular dysplasia); atrophy of affected kidney (can be surgically corrected)

Front 105

causes of essential HTN

Back 105

FMHx, African-American, diet (Na intake), obesity, stress, cigarette smoking, physical inactivity

Front 106

malignant HTN

Back 106

marked increase in Diastolic BP, focal retinal hemorrhages and papilledema, LVH, and LV failure

-most often in young black males, tho happens in <5% of pts w/high BP

Front 107

what are the renal changes caused by malignant HTN

Back 107

malignant nephrosclerosis

arterioles or glomerular capillaries rupture -> "flea-bitten" kidney (multiple pinpoint petechial hemorrhages on kidney surface; large swollen kidneys; necrotizing arteriolitis and glomerulitis w/fibrinoid necrosis)

hyperplastic arteriolosclerosis (affects both glomeruli and arterioles)